Integrin adhesion receptors facilitate the movement of blood borne cells into lymphoid and nonlymphoid tissue during both steady state and inflammatory conditions. In addition, integrins promote the stable interaction of T lymphocytes with antigen presenting cells that are necessary for optimal adaptive immune responses. Signal transduction initiated by antigen and chemokine receptors regulates the functional activity of integrin receptors to promote appropriate periods of strong adhesion during lymphocyte migration and antigen recognition. Recent advances in this area of immunological research have come from the identification of transgenic and knockout mouse models with defects in integrin function and/or T cell migration. These mouse models provide powerful new tools for elucidating the mechanisms by which integrin function and T cell migration are regulated. In addition, these models provide unique opportunities for examining the function of integrin-dependent responses in the context of physiological immune responses that can be initiated, manipulated, and monitored in mice.